本文選題：尿素通道蛋白B + 基因敲除��； 參考：《吉林大學(xué)》2010年碩士論文

【摘要】： 目的:以UT-B -/-小鼠為研究對(duì)象,對(duì)其心臟形態(tài)學(xué)變化、心肌肥大相關(guān)分子的表達(dá)水平進(jìn)行系列研究,以探討心肌肥大的發(fā)病機(jī)制。 方法:16周、52周UT-B -/-小鼠和野生型小鼠隨機(jī)分為四組。取小鼠心臟拍照、稱重,固定包埋行HE染色,觀察心臟形態(tài)學(xué)變化。取心臟蛋白勻漿液,Western blotting、RT-PCR檢測(cè)UT-B蛋白和mRNA的表達(dá)。應(yīng)用Real-time PCR檢測(cè)心臟組織心肌肥大相關(guān)分子ANP、BNP、α-actin的mRNA表達(dá)水平。取血清和心臟組織勻漿液檢測(cè)尿素含量。心臟組織勻漿液檢測(cè)NO含量。Western blotting、RT-PCR檢測(cè)eNOs表達(dá)水平。 結(jié)果: UT-B -/-老齡小鼠(52W)心臟體積增大, UT-B -/-老齡小鼠(52W)心臟系數(shù)明顯高于同齡野生型小鼠,UT-B -/-小鼠血清和心臟組織中尿素水平明顯高于UT-B +/+小鼠,UT-B -/-老齡小鼠(52W)增加更為明顯,52周UT-B -/-小鼠心臟ANP、α-actin的表達(dá)水平明顯增加, UT-B-/-小鼠心臟NO水平降低,該小鼠心臟eNOS的mRNA和蛋白表達(dá)水平明顯低于同齡野生型小鼠,以56周時(shí)更為明顯。 結(jié)論:UT-B基因敲除導(dǎo)致小鼠發(fā)生了心肌肥大。其機(jī)制可能是UT-B基因敲除導(dǎo)致小鼠血液和心肌組織中尿素含量升高,高于正常水平濃度的尿素影響心肌細(xì)胞的電生理功能,使心室肌細(xì)胞Na+通道電流和K+通道電流受到抑制,心肌細(xì)胞的興奮性和傳導(dǎo)性下降,加上長期高尿素內(nèi)環(huán)境對(duì)心肌細(xì)胞的應(yīng)激性負(fù)荷,及對(duì)內(nèi)源性NO產(chǎn)生的抑制作用,最后導(dǎo)致小鼠發(fā)生了心肌肥大,心肌肥大相關(guān)分子ANP、α-actin、SERCA2明顯增加。
[Abstract]:Aim: to study the changes of cardiac morphology and the expression level of cardiac hypertrophy related molecules in UT-B-r-mice in order to explore the pathogenesis of myocardial hypertrophy. Methods UT-B-r-r-and wild-type mice were randomly divided into four groups. The mice heart was photographed, weighed and immobilized for HE staining to observe the morphologic changes of the heart. The expression of UT-B and mRNA in heart homogenate was detected by RT-PCR. Real-time PCR was used to detect the expression of mRNA and 偽 -actin in cardiac hypertrophy. Serum and heart homogenate were taken to detect urea content. No content in heart homogenate was detected. RT-PCR was used to detect the expression of eNOs in heart tissue homogenate. Results: the heart volume of UT-B -r-aged mice increased, and the heart coefficient of UT-B -r-aged mice was significantly higher than that of UT-B / R mice of the same age. The levels of urea in serum and heart tissue of mice of the same age were significantly higher than those of UT-B / UT-B / R old mice. The expression of ANP- 偽 -actin in the heart of UT-B-/-mice was significantly increased, and the no level in the heart of UT-B-R-mice was decreased. The expression of mRNA and protein in the heart of the mice was significantly lower than that of the wild type mice of the same age, especially at 56 weeks. Conclusion the knockout of the 1: UT-B gene leads to cardiac hypertrophy in mice. The mechanism may be that knockout of UT-B gene leads to the increase of urea content in blood and myocardial tissue of mice. Urea at higher than normal level affects the electrophysiological function of cardiac myocytes and inhibits the Na and K channel currents in ventricular myocytes. The decrease of excitability and conductivity of cardiomyocytes, the stress load of long-term high urea environment on cardiomyocytes, and the inhibition of endogenous no production resulted in cardiac hypertrophy in mice. ANP- 偽-actinine SERCA2 increased significantly.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2010
【分類號(hào)】：R363

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

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2 張學(xué)新;孟艷;張文杰;趙春燕;趙雪儉;楊寶學(xué);;尿素通道蛋白B基因敲除小鼠心臟電生理特性的改變[J];中國應(yīng)用生理學(xué)雜志;2008年04期

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本文編號(hào)：1814033